Biomedical subjects

X Zhou

Publications and source records attributed to X Zhou.

At least 127 records · Page 7Linked to original sources

PubMed2001

Successful mismatched sibling cord blood transplant in Hb Bart's disease.

A 20-month-old girl with Hb Bart's disease, who had survived neonatal complications, underwent HLA-DR antigen mismatched sibling cord blood transplantation successfully. Immune thrombocytopenia, which occurred around 2.5 months after transplant, responded to intravenous gamma-globulin. The fetal hemoglobin level rose to a peak of 52.3% on day +69 post transplant and declined gradually during the following year. Ten percent of hemoglobin Bart's was detected 2 months after transplant and this reflects the alpha-thalassemia trait of the donor.

Female↗

PubMed2001

Identification of the ligand-binding domain of human vascular-endothelial-growth-factor receptor Flt-1.

The vascular-endothelial-growth-factor (VEGF) receptor Flt-1 has been shown to be involved in vasculogenesis and angiogenesis. The receptor is characterized by seven immunoglobulin-like loops within the extracellular domain and the first three N-terminal immunoglobulin-like loops are involved in high-affinity binding of VEGF. The minimal extracellular domains of Flt-1 to achieve VEGF binding were screened using the yeast two-hybrid system. The result showed that the binding capacity of loop2-3 was close to that of loop1-3. The two truncated mutants consisting of loop2-3 and loop1-3 were expressed in the methylotrophic yeast Pichia pastoris at high levels (0.3 g[corrected]/litre). The corresponding proteins, named soluble (s)Flt-1(2-3) and sFlt-1(1-3), were purified. An in vitro biological activity assay showed that the binding capacity of sFlt-1(2-3) to human VEGF(165) and the inhibiting effect of it on human umbilical-vein endothelial cell proliferation stimulated by human VEGF(165) were close to those of sFlt-1(1-3). Animal tests showed that sFlt-1(2-3) could significantly inhibit the formation of regenerated blood vessels stimulated by hVEGF(165).

Angiogenesis Inhibitors↗

PubMed2001

Expression and function of the HSD-3.8 gene encoding a testis-specific protein.

The nucleotide sequence of the full length HSD-3.8 cDNA (accession number AF311312), encoding a human sperm component, was determined to consist of 3818 bp with a reading frame of 2778 bp encoding a deduced polypeptide composed of 926 amino acids. A 0.7 kb fragment containing three immunological epitopes of HSD-3.8 cDNA was prepared and used to construct recombinant expression vectors. The constructs were transformed into E.coli BL-21, and the fusion proteins were expressed, isolated and purified. Using the polyclonal antibodies raised against the purified expressed fusion proteins, positive immunostaining occurred over the surface of the postacrosomal zone of human spermatozoa and of germ cells within the seminiferous epithelium of human testis. Intense staining of large pachytene primary spermatocytes occurred. The capacity of the recombinant protein to reduce fertility as an immunogen in adult female rats was assessed. Immunized animals were infertile or exhibited marked reduction in their fertility. Analysis of the deduced HSD-3.8 polypeptide revealed the presence of a tetratricopeptide repeat (TPR) motif, a P-loop sequence that acts as a binding site for ATP/GTP and phosphorylation sites for PKC, CK2 and cAMP/cGMP-dependent protein kinases. A blot overlay assay with [alpha-(32)P]GTP showed that the polypeptide encoded by the 0.7 kb fragment of HSD-3.8 is a GTP binding protein. It was also shown to possess GTPase activity and to be phosphorylated by PKC in vitro. In conclusion, HSD-3.8 is a GTP binding protein and its activity may be regulated by phosphorylation.

Adenosine Triphosphate↗

PubMed2001

ATP binding cassette transporter ABCA1 modulates the secretion of apolipoprotein E from human monocyte-derived macrophages.

Apolipoprotein E (apoE) produced by macrophages in the arterial wall protects against atherosclerosis, but the regulation of its secretion by these cells is poorly understood. Here we investigated the contribution of the adenosine triphosphate binding cassette transporters ABCA1 and ABC8 to the secretion of apoE from either primary human monocyte-derived macrophages (HMDM) or human THP1 macrophages. During incubations of up to 6 h, apoE secretion from both THP1 macrophages and HMDM was stimulated by 8-Br-cAMP, which activates ABCA1 expression. The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM. Antisense oligonucleotides directed against ABC8 mRNA also inhibited apoE secretion, although this inhibition was less pronounced and consistent than in the case of ABCA1. ApoE secretion from HMDM of ABCA1-deficient patients with Tangier disease was also decreased. ApoE mRNA expression was not affected by inhibition of ABCA1 or ABC8 in normal HMDM or the lack of functional ABCA1 in HMDM from Tangier disease patients. Inhibition of ABCA1 in HMDM prevented the occurrence of anti-apoE-immunoreactive granular structures in the plasma membrane. We conclude that ABCA1 and, to a lesser extent, ABC8 both promote secretion of apoE from human macrophages.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2001

Crystallization of agGST1-6, a recombinant glutathione S-transferase from a DDT-resistant strain of Anopheles gambiae.

Glutathione S-transferases (GSTs) belong to a family of detoxification enzymes that conjugate glutathione to various xenobiotics, thus facilitating their expulsion from the cell. GST activity is elevated in many insecticide-resistant insects, including the DDT-resistant malaria vector Anopheles gambiae. Crystals of the recombinant form of a GST from A. gambiae, agGST1-6, have been grown in at least five different crystal forms, with a broad range of diffraction resolution limits. A complete 2.0 A data set has been collected on a C-centered orthorhombic crystal form with unit-cell parameters a = 99.0, b = 199.4, c = 89.6 A. A search for heavy-atom derivatives has been initiated, along with phase-determination efforts by molecular replacement.

Animals↗

PubMed2001

Strain imaging and elasticity reconstruction of arteries based on intravascular ultrasound video images.

Based on intravascular ultrasound (IVUS) video images, a novel motion estimation method combining the genetic algorithm-based optical flow method and a step-by-step and sum strategy has been developed to estimate the displacement and strain distributions on the scan cross sections of the arteries. And then, real elasticity distributions were reconstructed under the conditions of small and large deformation. Experimental results of in vitro porcine arteries demonstrated the feasibility of the method. This investigation may have potentials to provide new technological means for monitoring and evaluating percutaneous transluminal coronary angioplasty procedure, especially, for the end users of IVUSpercimaging equipment.

Animals↗

PubMed2001

BSF binds specifically to the bicoid mRNA 3' untranslated region and contributes to stabilization of bicoid mRNA.

The early stages of Drosophila melanogaster development rely extensively on posttranscriptional forms of gene regulation. Deployment of the anterior body patterning morphogen, the Bicoid protein, requires both localization and translational regulation of the maternal bicoid mRNA. Here we provide evidence that the bicoid mRNA is also selectively stabilized during oogenesis. We identify and isolate a protein, BSF, that binds specifically to IV/V RNA, a minimal form of the bicoid mRNA 3' untranslated region that supports a normal program of mRNA localization during oogenesis. Mutations that disrupt the BSF binding site in IV/V RNA or substantially reduce the level of BSF protein lead to reduction in IV/V RNA levels, indicating a role for BSF in RNA stabilization. The BSF protein is novel and lacks all of the characterized RNA binding motifs. However, BSF does include multiple copies of the PPR motif, whose function is unknown but appears in other proteins with roles in RNA metabolism.

Amino Acid Sequence↗

PubMed2001

Digital optical imaging of green fluorescent proteins for tracking vascular gene expression: feasibility study in rabbit and human cell models.

PURPOSE: To investigate the feasibility of using a sensitive digital optical imaging technique to detect green fluorescent protein (GFP) expressed in rabbit vasculature and human arterial smooth muscle cells. MATERIALS AND METHODS: A GFP plasmid was transfected into human arterial smooth muscle cells to obtain a GFP-smooth muscle cell solution. This solution was imaged in cell phantoms by using a prototype digital optical imaging system. For in vivo validation, a GFP-lentivirus vector was transfected during surgery into the carotid arteries of two rabbits, and GFP-targeted vessels were harvested for digital optical imaging ex vivo. RESULTS: Optical imaging of cell phantoms resulted in a spatial resolution of 25 microm/pixel. Fluorescent signals were detected as diffusely distributed bright spots. At ex vivo optical imaging of arterial tissues, the average fluorescent signal was significantly higher (P <.05) in GFP-targeted tissues (mean +/- SD, 9,357.3 absolute units of density +/- 1,001.3) than in control tissues (5,633.7 absolute units of density +/- 985.2). Both fluorescence microscopic and immunohistochemical findings confirmed these differences between GFP-targeted and control vessels. CONCLUSION: The digital optical imaging system was sensitive to GFPs and may potentially provide an in vivo imaging tool to monitor and track vascular gene transfer and expression in experimental investigations.

Animals↗

PubMed2001

Lack of role for nitric oxide in cholinergic modulation of myocardial contractility in vivo.

Despite intensive investigation, the role of nitric oxide (NO) in cholinergic modulation of myocardial contractility remains unresolved. The left anterior descending coronary artery of 34 anesthetized, open-chest dogs was perfused via an extracorporeal circuit. Segmental shortening (SS) was measured with ultrasonic crystals and coronary blood flow (CBF) was measured with an ultrasonic flow transducer. An intracoronary infusion of ACh (20 microg/min) was performed, with CBF held constant, under baseline and during dobutamine, CaCl(2), or amrinone at doses increasing SS by approximately 50% (10 microg/min, 15 mg/min, and 300 microg/min ic, respectively). ACh-induced responses during dobutamine were also assessed following treatment with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microg/min ic for 15 min). The effects of sodium nitroprusside (SNP; 80 microg/min ic), an exogenous NO donor, bradykinin (2.5 microg/min ic), a nonmuscarinic releaser of endothelial NO, and bilateral vagal stimulation (before and after L-NAME) were evaluated during dobutamine. ACh had no effect on SS under baseline or during CaCl(2), but it decreased SS during dobutamine or amrinone (-23 +/- 4% and -30 +/- 5%, respectively). Vagal stimulation also reduced SS during dobutamine. L-NAME did not alter the ACh- or vagal-induced decreases in SS during dobutamine. Neither SNP nor bradykinin affected SS during dobutamine. In conclusion, ACh and vagal stimulation have a negative inotropic effect during stimulation of the beta-adrenergic receptors that is independent of NO. The persistence of this effect during amrinone suggests that a mechanism downstream from adenylate cyclase is involved.

Acetylcholine↗

PubMed2001

Increased CO(2) stimulates K/Rb reabsorption mediated by H-K-ATPase in CCD of potassium-restricted rabbit.

Apical H-K-ATPase in the cortical collecting duct (CCD) plays an important role in urinary acidification and K reabsorption. Our previous studies demonstrated that an H-K-ATPase mediates, in part, Rb reabsorption in rabbit CCD (Zhou X and Wingo CS. Am J Physiol Renal Fluid Electrolyte Physiol 263: F1134-F1141, 1992). The purpose of these experiments was to examine using in vitro microperfused CCD from K-restricted rabbits 1) whether an acute increase in PCO(2) and, presumably, intracellular acidosis stimulate K absorptive flux; and 2) whether this stimulation was dependent on the presence of a functional H-K-ATPase. Rb reabsorption was significantly increased after exposure to 10% CO(2) in CCD, and this effect was persistent for the entire 10% CO(2) period, whereas 10 microM SCH-28080 in the perfusate totally abolished the stimulation of Rb reabsorption by 10% CO(2). After stimulation of Rb reabsorption by 10% CO(2), subsequent addition of 0.1 mM methazolamide, an inhibitor of carbonic anhydrase, failed to affect Rb reabsorption. However, simultaneous exposure to 10% CO(2) and methazolamide prevented the stimulation of Rb reabsorption. Treatment with the intracellular calcium chelator MAPTAM (0.5 microM) inhibited the stimulation of Rb reabsorption by 10% CO(2). Similar inhibition was also observed in the presence of either a calmodulin inhibitor, W-7 (0.5 microM), or colchicine (0.5 mM), an inhibitor of tubulin polymerization. In time control studies, the perfusion time did not significantly affect Rb reabsorption. We conclude the following: 1) stimulation of Rb reabsorption on exposure to 10% CO(2) is dependent on the presence of a functional H-K-ATPase and appears to be regulated in part by the insertion of this enzyme into the apical plasma membrane by exocytosis; 2) insertion of H-K-ATPase requires changes in intracellular pH and needs a basal level of intracellular calcium concentration; and 3) H-K-ATPase insertion occurs by a microtubule-dependent process.

Absorption↗

PubMed2001

Influence of gender on upper airway mechanics: upper airway resistance and Pcrit.

It has been proposed that the difference in sleep apnea prevalence is related to gender differences in upper airway anatomy and physiology. To explain the prevalence difference, we hypothesized that men would have an increased upper airway resistance and increased critical closing pressure (Pcrit) compared with women. In protocol 1, resistance at two points, fixed flow of 0.2 l/s (RL) and peak flow (Rpk), was measured in 33 men and 27 women without significant sleep-disordered breathing. We found no difference in either RL (-6.9 +/- 5.9 vs. -8.6 +/- 8.2 cmH2O) or Rpk (-9.3 +/- 6.8 vs. -10.0 +/- 11.9 cmH2O) between the men and women. A multiple linear regression to correct for the effects of age and body mass index confirmed that gender had no effect on resistance. In protocol 2, Pcrit was measured in eight men and eight women without sleep-disordered breathing. We found no difference in Pcrit (-10.4 +/- 3.1 vs. -8.8 +/- 2.7 cmH2O) between men and women. We conclude that there are no significant differences in collapsibility between men and women. We present an unifying hypothesis to explain the divergent findings of gender differences in upper airway physiology.

Adult↗

PubMed2001

LDL immunization induces T-cell-dependent antibody formation and protection against atherosclerosis.

Atherosclerosis is an inflammatory disease, and the involvement of immune mechanisms in disease progression is increasingly recognized. Immunization with oxidized low density lipoprotein (LDL) decreases atherosclerosis in several animal models. To explore humoral and cellular immune reactions involved in this protection, we immunized apolipoprotein E knockout mice with either homologous plaque homogenates or homologous malondialdehyde (MDA)-LDL. Immunization with both these antigen preparations reduced lesion development. The plaques contained immunogen(s) sharing epitopes on MDA-LDL, MDA-very low density lipoprotein, and oxidized cardiolipin. This shows that a T-cell-dependent antibody response was associated with protection against atherosclerosis. The protection was associated with specific T-cell-dependent elevation of IgG antibodies against MDA-LDL and oxidized phospholipids, and the increased titers of IgG antibodies were correlated with decreased lesion formation and lower serum cholesterol levels.

Animals↗

PubMed2001

Angiotensin type 1 receptor antagonism and ACE inhibition produce similar renoprotection in N(omega)-nitro-L>-arginine methyl ester/spontaneously hypertensive rats.

This study was conducted to determine potentially differential effects between an angiotensin II type 1 (AT(1)) receptor antagonist and an ACE inhibitor on systemic, renal, and glomerular hemodynamics and pathological changes in spontaneously hypertensive rats (SHR) with N(omega)-nitro-L>-arginine methyl ester (L-NAME)-exacerbated nephrosclerosis. The hemodynamic, renal micropuncture, and pathological studies were performed in 9 groups of 17-week-old male SHR treated as follows: group 1, controls (n=16); group 2, candesartan (10 mg/kg per day for 3 weeks) (n=7); group 3, enalapril (30 mg/kg per day for 3 weeks) (n=8); group 4, candesartan (5 mg/kg per day) plus enalapril (15 mg/kg per day for 3 weeks) (n=9); group 5, L-NAME (50 mg/L in drinking water for 3 weeks) (n=17); group 6, L-NAME (50 mg/L) plus candesartan (10 mg/kg per day for 3 weeks) (n=7); group 7, L-NAME (50 mg/L) for 3 weeks followed by candesartan (10 mg/kg per day) for another 3 weeks (n=8); group 8, L-NAME (50 mg/L) plus enalapril (30 mg/kg per day for 3 weeks) (n=7); and group 9, L-NAME (50 mg/L) plus enalapril (30 mg/kg per day) and the bradykinin antagonist icatibant (500 microg/kg SC per day via osmotic minipump for 3 weeks) (n=7). Both candesartan and enalapril similarly reduced mean arterial pressure and total peripheral resistance index. These changes were associated with significant decreases in afferent and efferent glomerular arteriolar resistances as well as glomerular capillary pressure. Histopathologically, the glomerular and arterial injury scores were decreased significantly, and left ventricular and aortic masses also were diminished significantly in all treated groups. L-NAME-induced urinary protein excretion was prevented by both candesartan and enalapril. Thus, both AT(1) receptor and ACE inhibition prevented and reversed the pathophysiological alterations of L-NAME-exacerbated nephrosclerosis in SHR. Itatibant only blunted the antihypertensive effects of enalapril but did not attenuate the beneficial effects of ACE inhibition on the L-NAME-induced nephrosclerosis. Thus, the AT(1) receptor antagonism and ACE inhibition have similar renal preventive effects, which most likely were achieved through reduction in the effects of angiotensin II, and ACE inhibition of bradykinin degradation demonstrated little evidence of renoprotection.

Adrenergic beta-Antagonists↗

PubMed2001

Construction, expression, and characterization of recombinant hirudin in Escherichia coli.

The mutant gene of HV2-K47 was obtained by polymerase chain reaction-directed mutagenesis and expressed in Escherichia coli. Many elements that could affect its expression level were compared. The product was purified to homogeneity via three chromatographic steps--ion exchange, gel filtration, and reverse phase chromatography--on the AKTA Explorer System. The anti-thrombin activity of HV2-K47 is much higher than that of recombinant HV2. Some properties and expression conditions were investigated systematically, which would be useful for further studies of hirudin and other small proteins.

Cloning, Molecular↗

PubMed2001

IGFs and IGF-binding proteins in short children with steroid-dependent nephrotic syndrome on chronic glucocorticoids: changes with 1 year exogenous GH.

OBJECTIVE: Children with steroid-dependent nephrotic syndrome (SDNS), despite being in remission on glucocorticoids, continue to have growth retardation and short stature. The mechanism is uncertain as both chronic glucocorticosteroids and the nephrotic syndrome may independently affect growth. We investigated the changes in the IGFs and IGF-binding proteins (IGFBPs) in a group of short SDNS children, and studied the changes prospectively with 1 year's treatment with GH. DESIGN AND METHODS: Total and 'free' IGF-I, IGFBP-3 and acid-labile subunit (ALS) were studied in eight SDNS boys (mean age=12.6 years; mean bone age=9.1 years) on long term oral prednisolone (mean dose 0.46 mg/kg per day) before, during, and after, 1 year's treatment with GH (mean dose 0.32 mg/kg per week). Pretreatment comparisons were made with two control groups, one matched for bone age (CBA; mean bone age=9.2 years), and another for chronological age (CCA; mean chronological age=13 years). Subsequently, three monthly measurements of serum and urine IGFBPs were carried out in the GH-treated SDNS patients using Western ligand blot and Western immunoblot. RESULTS: Pre-treatment serum total IGF-I levels and the IGF-I/IGFBP-3 ratio were elevated significantly in SDNS compared with CBA, and were similar to CCA. Serum free IGF-I levels were elevated significantly compared with both control groups, but serum IGFBP-3 did not differ significantly. Urinary IGFBP-2, IGFBP-3 and ALS were detectable in the SDNS children only. With GH treatment, IGF-I and IGFBP-3, but not IGF-II, increased significantly compared with pre-treatment values, and returned to baseline after cessation of GH treatment. Urinary IGFBPs did not change significantly with GH treatment. CONCLUSIONS: There is persistent urinary loss of IGFBP-2, IGFBP-3 and ALS in children with SDNS in remission with growth retardation. However, the significant elevation in serum IGF-I suggests that glucocorticoid-induced resistance to IGF is the main factor responsible for the persistent growth retardation in these children. Exogenous GH was able to overcome this resistance by further increasing serum IGF-I.

Adolescent↗

PubMed2001

Expression changes of activin A in the development of hepatic fibrosis.

AIM: To examine the expression of activin A, a member of the transforming growth factor (TGFbeta) superfamily, recently has been reported to be overexpressed in liver cirrhosis, in the course of carbon tetrachloride-induced rat hepatic fibrosis. METHODS: Hepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. At the end of 1, 2, 3, 4, 5, 6 and 7 weeks after carbon tetrachloride injections, the rats were killed in group (6-10 rats each time) for study. The activin A messenger RNA expression and its protein localization were assessed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: The normal rat liver expressed activin A mRNA and protein, and its expression was transiently decreased and became undetectable after carbon tetrachloride injections for 2 or 3 weeks and then increased gradually. After injection of carbon tetrachloride for 6 and 7 weeks, activin A mRNA and protein expressions were significantly enhanced in rat liver. Compared with that of the normal rat liver. Activin A mRNA expression levels in rats receiving carbon tetrachloride injections for 6 and 7 weeks were 1.6 and 2.2 times that of those in normal rat liver respectively (0.456 +/- 0.094 vs 0.2860.0670, P< 0.01; 0.620 +/- 0.134 vs 0.286 +/- 0670, P< 0.01). Immunohistochemistry showed that activin A expressed in hepatocytes of normal liver, and its expression was decreased in rats receiving carbon tetrachloride for 2 or 3 weeks. Compared with normal liver, activin A expression distribution mode changed in fibrotic liver, being increased significantly in hepatocytes around fibrotic areas. CONCLUSION: Activin A expression was increased in late stage of hepatic fibrosis, and this may be involved in hepatic fibrosis formation in this period.

Activins↗

PubMed2001

Effect of bowel rehabilitative therapy on structural adaptation of remnant small intestine: animal experiment.

AIM: To investigate the individual and the combined effects of glutamine, dietary fiber, and growth hormone on the structural adaptation of the remnant small bowel. METHODS: Forty-two adult male Sprague-Dawley rats underwent 85% mid-small bowel resection and received total parenteral nutrition (TPN) support during the first three postoperational days.From the 4th postoperational day, animals were randomly assigned to receive 7 different treatments for 8 days: TPNcon group, receiving TPN and enteral 20 g x L(-1) glycine perfusion; TPN+Gln group, receiving TPN and enteral 20 g x L(-1) glutamine perfusion; ENcon group, receiving enteral nutrition (EN) fortified with 20 g x L(-1) glycine; EN+Gln group, enteral nutrition fortified with 20 g x L(-1) glutamine; EN+Fib group, enteral nutrition and 2 g x d(-1) oral soybean fiber; EN+GH group, enteral nutrition and subcutaneous growth hormone (GH) (0.3 IU) injection twice daily; and ENint group, glutamine-enriched EN, oral soybean fiber, and subcutaneous GH injection. RESULTS: Enteral glutamine perfusion during TPN increased the small intestinal villus height (jejunal villus height 250 microm +/- 29 microm in TPNcon vs 330 microm +/- 54 microm in TPN+Gln, ileal villus height 260 microm +/- 28 microm in TPNcon vs 330 microm +/- 22 microm in TPN+Gln, P<0.05) and mucosa thickness (jejunal mucosa thickness 360 microm +/- 32 microm in TPNcon vs 460 microm +/- 65 microm in TPN+Gln, ileal mucosa thickness 400 microm +/- 25 microm in TPNcon vs 490 microm +/- 11 microm in TPN+Gln,P< 0.05) in comparison with the TPNcon group. Either fiber supplementation or GH administration improved body mass gain (end body weight 270 g +/- 3.6g in EN+Fib, 265.7 g +/- 3.3 g in EN+GH, vs 257 g +/- 3.3 g in ENcon, P< 0.05), elevated plasma insulin-like growth factor (IGF-I) level (880 microg x L(-1). 52 microg x L-(-1) in EN+Fib,1200 microg x L(-1). 96 microg x L-(-1) in EN +/- GH, vs 620 microg x L(-1).43 microg x L-(-1) in ENcon, P< 0.05), and increased the villus height (jejunum 560 microm +/- 44 microm in EN +/- Fib, 530 microm +/- 30 microm in EN +/- GH, vs 450 microm +/- 44 microm in ENcon, ileum 400 microm +/- 30 microm in EN+Fib, P<0.05) and the mucosa thickness (jejunum 740 microm +/- 66 microm in EN +/- Fib, 705 microm +/- 27 microm in EN +/- GH, vs 608 microm +/- 58 microm in ENcon, ileum 570 microm +/- 27 microm in EN +/- Fib, 560 microm +/- 56 microm in remnant jejunum and ileum. Glutamine-enriched EN produced little effect in body mass, plasma IGF-I level, and remnant small bowel mucosal structure. The ENint group had greater body mass (280 g +/- 2.2g), plasma IGF-I level (1450 microg x L(-1). 137 microg x L-(-1)), and villus height (jejunum 620 microm +/- 56 microm, ileum 450 microm +/- 31 microm) and mucosal thickness (jejunum 800 microm +/- 52 microm, ileum 633 microm +/- 33 microm) than those in ENcon, EN+Gln (jejunum villus height and mucosa thickness 450 microm +/- 47 microm and 610 +/- 63 microm, ileum villus height and mucosa thickness 330 microm +/- 39 microm and 500 microm +/- 52 microm), EN+GH groups (P<0.05), and than those in EN+Fib group although no statistical significance was attained. CONCLUSION: Both dietary fiber and GH when used separately can enhance the postresectional small bowel structural adaptation. Simultaneous use of these two gut-trophic factors can produce synergistic effects on small bowel structural adaptation. Enteral glutamine perfusion is beneficial in preserving small bowel mucosal structure during TPN, but has little beneficial effect during EN.

Adaptation, Physiological↗

PubMed2001

[Using fluorescence PCR analysis for early diagnosis and carriers detection of Chinese Wilson's disease].

OBJECTIVE: To diagnose the pre-symptomatic cases of Chinese Wilson's disease(WD) and detect the potential carriers by using fluorescence PCR technique. METHODS: Screening the high frequency spot Arg778Leu of WD gene mutation in 66 Chinese WD patients, 55 healthy family members and 30 controls, and selecting 3 random samples (2 from WD patients, 1 from controls) for DNA sequencing to testify the accuracy of fluorescence PCR. RESULTS: Among 66 Chinese WD cases, 5 were found homozygous for mutation of Arg778Leu and 21 were compound heterozygous; the gene mutation rate was totally 39.4%. Out of 55 healthy family members, 12 were found heterozygous, and it was confirmed that 11 of these 12 individuals were WD gene carriers but not pre-symptomatic patients. The results of direct DNA sequencing consisted with those results detected by fluorescence PCR. CONCLUSION: The Arg778Leu mutation in exon 8 is the high frequency spot of Chinese Wilson's disease gene. Fluorescence PCR analysis is a rapid, accurate gene diagnostic method and demonstrates a high detecting rate.

Adolescent↗